What you carry at this position in your DNA and what research says about it.
Fatty Acid Metabolism: 9/10 evidence, 22 publications.
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Sample genotype (not yours): C/C
Efficient Fatty Acid Conversion with Higher Cardiovascular Risks
Efficient conversion of plant-based fats into active omega-3 and omega-6 fatty acids occurs with this genotype. However, this rapid processing also increases the production of pro-inflammatory compounds and elevates blood clot risks.
What this genotype means: Elevated blood clot risk; Higher triglyceride levels; Efficient conversion of plant omega-3s.
Sample genotype (not yours): C/G
Typical Fatty Acid Conversion and Balanced Cardiovascular Risk
Balanced conversion of dietary fats maintains typical levels of both precursor and long-chain fatty acids. Cardiovascular and inflammatory risks remain at baseline levels.
What this genotype means: Typical fatty acid conversion rates; Baseline cardiovascular risk profile; Balanced inflammatory potential.
Sample genotype (not yours): G/G
Lower Inflammatory Potential with Slower Omega-3 Conversion
Reduced production of pro-inflammatory arachidonic acid lowers blood clot risk and LDL cholesterol. However, converting plant-based omega-3s into active forms is highly inefficient.
What this genotype means: Lower blood clot and triglyceride risk; Inefficient conversion of plant-based omega-3s; Slightly elevated LDL cholesterol.
Gene function and biological role
Gene Function: Fatty acid desaturase 1, encoded by the FADS1 gene, is a key enzyme in the biosynthesis of long-chain polyunsaturated fatty acids [1]. It catalyzes the conversion of dihomo-gamma-linolenic acid into arachidonic acid, an essential precursor for inflammatory mediators [1]. The enzyme also plays a critical role in converting plant-derived alpha-linolenic acid into eicosapentaenoic acid [1]. Variations in this gene significantly influence circulating lipid levels and cardiovascular health [2].
Variant Impact: Located in the 3 prime untranslated region of the FADS1 gene, rs174545 is a common genetic variant that regulates enzyme expression [3]. This genetic change alters the rate of delta-5 desaturase activity, directly impacting how the body processes dietary fats [2]. The major C allele is linked to higher enzyme levels and rapid conversion of short-chain fatty acids [3]. Conversely, the minor G allele reduces desaturase activity, leading to a slower conversion rate [3].
Key Insight: This variant acts as a metabolic dial, determining whether your body easily converts plant-based omega-3s into active forms or requires direct marine sources.
Location: FADS1. Chromosome 11 · 11q12.2 · 61.8 Mb
Origin Story: The high-activity C allele became highly advantageous during the transition to agriculture in Europe around 8,500 years ago, allowing early farmers to synthesize essential long-chain fatty acids from a plant-heavy diet.
Estimated prevalence by population
Global 52.9%; European 44.1%; African 85.0%; East Asian 19.8%; South Asian 67.4%; Americas 26.2%; Ashkenazi 50.9%; Finnish 33.7%; Middle Eastern 42.7%; Amish 58.7%.
Estimated CC genotype frequency.
Global 36.7%; European 44.6%; African 14.4%; East Asian 49.4%; South Asian 29.4%; Americas 50.0%; Ashkenazi 40.9%; Finnish 48.7%; Middle Eastern 45.3%; Amish 35.8%.
Estimated CG genotype frequency.
Global 10.4%; European 11.3%; African 0.6%; East Asian 30.9%; South Asian 3.2%; Americas 23.8%; Ashkenazi 8.2%; Finnish 17.6%; Middle Eastern 12.0%; Amish 5.5%.
Estimated GG genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Blood Clot Risk. Evidence: 6/10. Source: PMID 36777996. Increased Risk.
Lipids & Cholesterol
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Reduced.
LDL Cholesterol. Evidence: 9/10. Source: PMID 38448586. Elevated.
Nutrition & Metabolism
Macronutrient Metabolism
Arachidonic Acid Levels. Evidence: 6/10. Source: PMID 25500335. Elevated.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18320251. Efficient.
Showing effects for C/G genotype
Blood Clot Risk. Evidence: 6/10. Source: PMID 36777996. Typical Risk.
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Typical.
LDL Cholesterol. Evidence: 9/10. Source: PMID 38448586. Typical.
Arachidonic Acid Levels. Evidence: 6/10. Source: PMID 25500335. Typical.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18320251. Typical.
Showing effects for G/G genotype
Blood Clot Risk. Evidence: 6/10. Source: PMID 36777996. Lower Risk.
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Elevated.
LDL Cholesterol. Evidence: 9/10. Source: PMID 38448586. Reduced.
Arachidonic Acid Levels. Evidence: 6/10. Source: PMID 25500335. Reduced.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18320251. Reduced.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Efficient synthesis of long-chain polyunsaturated fatty acids is driven by high delta-5 desaturase activity [1]. This rapid conversion leads to elevated circulating levels of arachidonic acid, a key building block for inflammatory signaling molecules [1]. Consequently, higher LDL cholesterol and an increased risk of venous thromboembolism are commonly observed [2] [3]. While plant-based omega-3 sources like flaxseed are easily converted into active EPA, the overall metabolic profile leans toward higher systemic inflammation [1]. Balancing dietary intake by reducing omega-6-rich seed oils may help mitigate these cardiovascular risks [4].
Elevated blood clot risk; Higher triglyceride levels; Efficient conversion of plant omega-3s.
Sample genotype: CG (Heterozygous)
Intermediate delta-5 desaturase activity provides a balanced rate of fatty acid conversion [1]. Levels of arachidonic acid and plant-derived precursors like linoleic acid remain within the typical range [1]. This moderate processing rate avoids both the high inflammatory potential of rapid conversion and the poor synthesis efficiency of slow conversion [2]. Baseline risks for triglycerides, LDL cholesterol, and venous thromboembolism are maintained [3] [4] [5]. Standard dietary guidelines for balanced omega-3 and omega-6 intake are generally sufficient for maintaining cardiovascular health [6].
Typical fatty acid conversion rates; Baseline cardiovascular risk profile; Balanced inflammatory potential.
Sample genotype: GG (Homozygous)
Slower delta-5 desaturase activity significantly limits the conversion of short-chain fatty acids into longer forms [1]. This slow processing results in lower levels of arachidonic acid, which reduces the baseline potential for systemic inflammation [1]. Benefits include lower LDL cholesterol and a reduced risk of venous thromboembolism [2] [3]. However, converting plant-derived alpha-linolenic acid into active EPA and DHA is highly inefficient [1]. Additionally, triglyceride levels tend to run slightly higher with this genotype [4]. Obtaining pre-formed EPA and DHA directly from marine sources like fish oil bypasses this metabolic bottleneck [5].
Lower blood clot and triglyceride risk; Inefficient conversion of plant-based omega-3s; Slightly elevated LDL cholesterol.
Variants with shared genetic architecture
rs174546 · FADS1 Gene · Chr 11 · Fatty Acid Metabolism
rs174554 · FADS1 Gene · Chr 11 · Omega Fat Conversion
rs174550 · FADS1 Gene · Chr 11 · Omega Fatty Acid Processing
Genetic variation in lipid desaturases and its impact on the development of human disease.
Global Biobank Meta-analysis Initiative: Powering genetic discovery across human disease.
Genome-wide characterization of circulating metabolic biomarkers.
Content updated August 2026.
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